Translational approaches: From fatty liver to non-alcoholic steatohepatitis

作     者：Natalia Rosso Norberto C Chavez-Tapia Claudio Tiribelli Stefano Bellentani 

作者机构：Fondazione Italiana Fegato34149 Trieste Italy Obesity and Digestive Diseases UnitMédica Sur Clinic and FoundationMexico 14050 México Department of Medical SciencesUniversity of Trieste Department of Gastroenterology and EndoscopyAzienda USL di ModenaOspedale "Ramazzini" 41012 Carpi (Modena) Italy 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2014年第20卷第27期

页      面：9038-9049页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Supported by European Union Seventh Framework Program(FP7/2007-2013)under grant agreement,No.Health-F2-2009-241762,for the project FLIP Italian National Grant MIUR(Art.13 D.LGS 297/99-Progetto Nutrizione e Salute) an in house grant from Fondazione Italiana Fegato,ONLUS 

主　　题：Fatty Liver Obesity Metabolic syndrome Inflammation In vitro Experimental model 

摘      要：Over the past few decades, non-alcoholic fatty liver disease(NAFLD) has become one, if not the most common,cause of chronic liver disease affecting both adults and children. The increasing number of cases at an early age is the most worrying aspect of this pathology, since it provides more time for its evolution. The spectrum of this disease ranges from liver steatosis to steatohepatitis, fibrosis and in some cases, hepatocellular carcinoma. NAFLD may not always be considered a benign disease and hepatologists must be cautious in the presence of fatty liver. This should prompt the use of the available experimental models to understand better the pathogenesis and to develop a rational treatment of a disease that is dangerously increasing. In spite of the growing efforts, the pathogenesis of NAFLD is still poorly understood. In the present article we review the most relevant hypotheses and evidence that account for the progression of NAFLD to non-alcoholic steatohepatitis(NASH) and fibrosis. The available in vitro and in vivo experimental models of NASH are discussed and revised in terms of their validity in translational studies. These studies must be aimed at the discovery of the still unknown triggers or mediators that induce the progression of hepatic inflammation, apoptosis and fibrosis.